Salt, sugar, and the search for the root of all evil

Two interesting articles appeared in the New York Times earlier this week, one on salt and the other on sugar. In both cases, it’s the responses rather than the research itself that are most interesting, because they nicely illustrate the confusion and contradictions that result from our endless quest to identify a single Nutritional Villain while ignoring the broader dietary and lifestyle contexts.

First, the salt. I blogged last fall about a study that found that salt intakes in Western diets haven’t changed over the past half-century, despite claims that salt is responsible for the epidemic rise in hypertension. Now a new JAMA study measured sodium levels in the urine of 3,681 healthy people over a 24-hour period (the most reliable way to determine salt intake), and then followed them for an average of 7.9 years. They found little effect on blood pressure, no effect on the risk of hypertension, and — surprisingly — those who ate less salt were more likely to die. Here’s the data showing the risk of death and non-fatal cardiovascular disease, divided into low, medium and high salt consumers:

Interesting stuff. But even more interesting is the how eager everyone in the Times article seems to be to discredit the findings. Now, criticism of studies is certainly fair game. But instead of checking for flaws in the methodology to decide whether the findings are legit, the approach here seems to start with looking at the findings and then (since they run counter to orthodoxy) deciding that the methodology must have been flawed. The only really substantive criticism aimed at the data is the following:

But among the study’s other problems, Dr. Briss said, its subjects who seemed to consume the smallest amount of sodium also provided less urine than those consuming more, an indication that they might not have collected all of their urine in an 24-hour period.

Okay, so I can see two possible hypotheses to explain this apparent anomaly:

Among the apparently healthy volunteers, those who had a premonition that they would die prematurely several years later were also disproportionately more likely to withhold some of their urine from the study in order to artificially reduce the amount of salt they were apparently consuming. Perhaps some underlying confounder explains it: the same character flaw that led them to hide their urine also led to the poor health decisions that eventually killed them.

People who eat lots of salt get more thirsty, drink more, and thus provide more urine.

I’m not saying the study is definitive or without flaws. It’s relatively small, and its subjects were young and healthy — the authors are careful to note that it doesn’t mean that reducing salt intake isn’t useful to reduce blood pressure for patients who already have high blood pressure. But the point is that the establishment response to an interesting new study isn’t “How do we explain this new data?”, it’s “How do we dismiss it?” And that’s a problem.

The sugar article, by Gretchen Reynolds, is essentially aimed as a corrective in the ongoing debate about “toxic fructose,” stirred most recently by Gary Taubes’s Times magazine article. Reynolds sums up some of the recent research on how fructose can help endurance athletes both during and after exercise. In other words, fructose is actually quite useful in some contexts. The responses below the article are quite interesting; e.g.:

While interesting, how is this article RELEVANT to the general audience that reads the NYT? The study referenced in the article relates how sugar affected “highly trained” athletes, a group that measures less than 1% of the population…

But it is relevant. Because it suggests what we really mean is not “Sugar is toxic,” but rather “Excessive sugar in the context of a sedentary lifestyle is toxic.” The first statement is a more attractive one, because it means we have a simple, well-defined enemy to attack, so all we have to do is engineer a bunch of Lo-Sugar snack foods and we’ll all be healthy again. Unfortunately, I think that’s a false promise. You can’t ignore the overall dietary and lifestyle context.

Isn’t there a large middle ground between a sedentary lifestyle and endurance runners? Should everyone be an endurance runner (no snark intended)?

I agree that the argument about salt is, for the most part, ridiculous. Artery inflammation from other substances making your body use cholesterol to “heal” the arteries has a higher effect on blood pressure than simple salt levels.

Seriously, I agree that (a) there’s a big middle ground, and (b) not everyone wants to be an endurance runner. Fair enough. And I absolutely agree that, if you decide you don’t want to exercise that much, you should be very careful about your added sugar intake.

What I’m reacting against is the leap from there to saying that “sugar is toxic.” It feels like we’re sitting in a fancy recording studio, and every 10 minutes some new guy walks into the control room and says “Oh my god, I’ve figured it out, it’s all about the treble! If you turn the treble down, this recording will sound awesome!” And so we turn the treble right down to zero, and the recording sucks. And the next guy comes in and tells us that it’s all about reverb, or bass, or noise reduction, or volume, or whatever. And every time someone suggests a new “answer,” we turn that knob all the way up or all the way down, and scratch our heads when it doesn’t fix everything. Our bodies are even more complicated than sound engineering. All (or at least a very large number) of the knobs matter.

I don’t think you need to be some sort of extremist endurance athlete to benefit from the judicious consumption of sugar. Plenty of ordinary folks go hiking; on a bad weather day in the Presidentials, for instance, a little sugar could be the difference between life and death.

Very interesting graphs. I do wonder about the following:
- high urine sodium may be a marker of healthy kidneys and means of dealing with sodium load rather than a marker of sodium consumption
- on the other hand, I would expect a relatively low urine sodium in, say, someone with heart failure (due to kidney under-perfusion and increased sodium reabsorption), or in someone with hypertensive damage to the kidneys (leading to decreased glomerular filtration); therefore in my mind the connection between between low urine sodium and cardiovascular morbidity and mortality doesn’t seem all that counter-intuitive